Consequences of Alzheimer's Disease

Amyloid-beta(M) plaques are bordered to overproduction of Aβ peptides by the brain that are close to the pathology of Alzheimer's disease. It is seen that Aβ132 and some of its forms combine to become bitter soluble all through changes within the cells. Such formations will not allow normal cells to...

Amyloid-beta(M) plaques are bordered to overproduction of Aβ peptides by the brain that are close to the pathology of Alzheimer's disease. It is seen that Aβ132 and some of its forms combine to become bitter soluble all through changes within the cells. Such formations will not allow normal cells to function effectively, propagate the neurons and cause action to return. The immune cells surrounding the nervous system, including microglia and astrocytes, try to get rid of the Aβ, but they might also assist in constructing the plaque. The actions of the microglia, for example, the secretion of Aβ-fibril-promoting pro-inflammatory cytokines, can enhance the Aβ polymerization process. Overexpression of Aβ in astrocytes and other specific genetic conditions such as ApoE deficiency limit the efflux of Aβ. This detrimental imbalance leads to further increase in inflammation and formation of plaques which drives neurodegenerative diseases. In Alzheimer\'s disease, tau proteins lose stability because they become hyperphosphorylated which means accumulation of too many phosphate groups. This phosphorylated tau then binds to its principal role of stabilizing microtubules which are essential components for transport within neurons. All of these are acquired changes that lead to tau delocalization from microtubules and subsequent microtubule collapse. Then these hyperphosphorylated tau proteins aggregate becoming neurofibrillary tangles within the neuronal cells. The tangles disrupt the normal inner workings of the cells and lead them towards death. Tauopathy can also propagate from one cell to another, thus exacerbating disease progression.